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作 者:金艳[1] 陈琪[2] 魏恩会[2] 蒋莉[2] 范乐明[2] 王南[2] 陈秀英[2]
机构地区:[1]无锡市第二人民医院心血管内科,无锡214002 [2]南京医科大学动脉粥样硬化研究中心,南京210029
出 处:《生物化学与生物物理学报》2001年第1期142-146,共5页
基 金:国家自然科学基金资助项目!No.39870363&&
摘 要:为研究清道夫受体与细胞内酪氨酸蛋白激酶的关系 ,用酪氨酸蛋白激酶抑制剂genistein处理人U937细胞。分别测定对照组和处理组细胞对碘标记的氧化低密度脂蛋白 [12 5I]ox LDL的结合、降解以及细胞内脂质蓄积的程度 ;并利用放射自显影的方法观察药物对细胞表面受体数目的影响 ,利用RT PCR法进一步探讨药物作用的分子机制。结果发现 genistein可以抑制细胞表面结合 [12 5I]ox LDL ,抑制细胞表面受体的表达以及细胞内降解[12 5I]ox LDL ,抑制细胞内胆固醇酯的蓄积 ,并且抑制SR AmRNA的转录 ,提示清道夫受体的活性可能与细胞内蛋白质酪氨酸磷酸化水平密切相关 ,genistein所引起的酪氨酸磷酸化水平下降可影响SRIn order to investigate the relationship between scavenger receptor type A and cell signal transduction, human U937 macrophages were treated with tyrosine protein kinase inhibitor genistein, then the cells were incubated with [ 125 I]ox LDL or ox LDL, and the cellular degradation of [ 125 I]ox LDL or binding were measured separately. Then the effect of the drug on cell surface expression of SR A were measured by means of autoradiography, it was found that genistein could reduce cellular SR A mRNA transcription by RT PCR. The results indicated that genistein could reduce U937 macrophages to bind lipids and reduce SR A expression by suppression of transcription, and could reduce degradation of lipids by U937 macrophage and accumulation of cholesterol within the cells. It suggests that the function of scavenger receptors may be correlated with cell tyrosine protein kinase, the mechanism is transcriptional and it also suggests that SR A may participate in the signal transduction directly.
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